Objective To investigate the effect of propofol on N-methyl-D-aspartate (NMDA) receptor-mediated currents. Methods Hippocampal neurons were prepared from newborn Wistar rats and cultured for 8-12 days. Whole cell currents were recorded using patch-clamp technique and cells were voltaged-clamped at - 80 mV. 100 ?mol?L-1 NMDA and 3 or 48 ?g?ml-1 propofol were applied with a multi-pipe ejection system. GABAA receptor was then blocked with 100 ?mol?L-1 bicuculline to investigate the effect of propofol on NMDA receptor without the influence of GABAA receptor.Results Run-down of INMDA induced by 100 ?mol?L-1 NMDA applied to neurons which were cultured for 8-12 days was 15%?8%. Propofol 3 or 48 ?g?ml-1 significantly inhibited spontaneous excitatory postsynaptic currents and elicited a Cl- -mediated response by direct activation of GABAA receptor in the absence of GABA. therefore produced a reversible inhibition of whole cell currents activated by NMDA. After the GABAA receptor was blocked by 100 ?mol?L-1 bicuculine propofol still inhibited NMDA currents slightly. Conclusion Propofol inhibits the NMDA subtype of glutamate receptor mainly through activation of GABAA receptor. It can also directly suppress the NMDA receptor slightly.

Objective To establish an in vitro oxygen-glucose deprivation/reoxygenation axon injury model in rat hippocampal neurons in order to found a basis for research concerning the injury of oxygen glucose deprivation and axons regeneration. MethodsThe hippocampal neurons isolated from rats 24 h after born and cultured for 7 d were exposed to D-hanks solution with nitrogen gas instead of the original culture medium for 0.5, 1.0 and 1.5 h respectively, and then continue to be cultured in the original culture medium with oxygen. LDH content in the culture media was measured at 1, 5, 24, 48 and 72 h after reoxygenation. The morphological changes of neuron and axon were observed with inverted phase contrast microscopy. ResultsAfter oxygen-glucose deprivation/reoxygenation injury, hippocampal neurons became darker, swollen, and were with shorten axons. With the elapse of time, the LDH content was increased. The survival rate of hippocampal neurons was higher and the change of axon length was more obvious in the group of oxygen-glucose deprivation for 0.5 h than in the other groups. ConclusionAn in vitro oxygen-glucose deprivation/reoxygenation axon injury model in rat hippocampal neurons is successfully established.

Scientific research training program is an important component in the 8-year medical education program. It focuses on the training of scientific research thinking and research methods. It is necessary to establish an effective evaluation system in order to achieve the learning outcomes of scientific research training program. PUMC has established an effective evaluation system which involves research project selecting,supervising,formative assessment,oral defense. This paper introduces the evaluation system of scientific research training program at PUMC.

Aim To investigate the protective effects of etomidate on cultured rat hippocampal neurons subjected to anoxia injury and its mechanism.Methods Hippocampal neurons of neonatal rat,which had been cultured in vitro for 10 days,were allocated to control groups and etomidate-treating groups.The neurons were exposed to oxygen-glucose deprivation for 24 h.The cell survival rate in each group was evaluated using MTT colorimetry.To explore the effect of etomidate on neuronal calcium overload evoked by anoxia or 50 mmol?L~(-1) KCl or 1 mmol?L~(-1) glutamate,fluo-3,a fluorescent probe,was used for imaging of intracellular calcium in laser scanning confocal microscope(LSCM)to measure real-time changes of [Ca~(2+)]_i in cultured rat hippocampal neurons.Results The hippocampal neurons developed acute neuronal swelling and widespread neuronal degeneration following anoxia for 24 h.Etomidate at concentrations of 1.2～4.8 mg?L~(-1) attenuated the neuronal injury in a dose-dependent manner(P

Objective To characterize the nasal resonance of children with spastic cerebral palsy by comparing it with that of ordinary school-age children.Methods The mean nasalance scores (MNSs) of 90 normal school-age children and 62 school-age children with spastic cerebral palsy were measured and compared.Results (1) Age has significant effects on the MNS of/a/,/i/and/m/ in ordinary children,but has almost no effect on the MNS of/u/.The MNS of/a/,/i/,/u/ and/m/ in children with spastic cerebral palsy does not change with age.(2) Sex only has a significant relationship with the MNS of/i/ in ordinary children,but does not significantly predict the other MNSs.(3) The MNS of/a/ of children with spastic cerebral palsy is significantly lower than that of ordinary children,and their MNS of/i/ and /u/ is significantly greater than those of ordinary children.Conclusions The MNS of /a/,/i/and /u/first increases and then decreases with age in ordinary children,while the MNS of/m/ increases gradually.Children with spastic cerebral palsy did not show the same trends and demonstrated a state of retardation of nasal resonance.Children with spastic cerebral palsy are more likely to display hypernasality than ordinary children.

Objective To apply data mining to risk prediction of sudden deafness, and form the association rules.Methods The clinical data of 517 patients with sudden deafness was collected, including the characteristics of 19 attributes: sex, age, season, hypertension, diabetes, heart disease, hypercholesterolemia, atherosclerosis, long-term smoking, alcoholism, mental tension, insomnia, weakness, bedridden, infection, congenital malformation, trauma, tumour and autoimmune diseases. The source database were cleaned, then mapped for mining database. Minimum support to 0.1 and minimum confidence level to 0.9 were set for analysis of association rules. Results One hundred and six strong association rules were formed, and the rules contained the relation between the incidence of sudden deafness and the characteristics of 19 attributes. Conclusion This method is conducive to make the abstract theory of mathematical statistics into useful association rules to guide the practice of disease prevention and control.

Objective To determine if propofol can protect cultured rat hippocampal neurons from anoxia-induced injury and elucidate the underlying mechanism.Methods Neonatal Wistar rats were decapitated. Hippocampus was isolated, minced and digested with 0.125 % trypsin at 371 for 25 min, then centrifuged at 1000 r/min for 5 min. The supernatant was discartled and the precipitate was resuspended in growth medium. The cell suspension was incubated at 37 ℃ for 10 days. The cultured hippocampal neurons were randomly divided into 3 groups: control group(group C) ,anoxia group(group A), propofol + anoxia group (group PA) . Group PA was further divided into 3 subgroups of different end-propofol concentrations:3, 12,48 mg?L-1 . The cultured neurons were transferred to low glucose medium and incubated at 37 ℃ in closed incubator filled with anoxic atmosphere (95% N2-5% CO2) for 24 h in group A and group PA (following addition of propofol) . The cell survival rate in each group was measured by MIT colorimetry. The real-time changes in [Ca2+ ]i in cultured hippocampal neurons induced by anoxia or glutamate or KCL were measured by fluorescence and laser scan confocal microscopy ( LSCM) after staining with fluo-3/AM.Results The hippocampal neurons developed acute swelling and widespread degeneration following anoxia. Propofol attenuated the neuronal injury at 12 and 48 mg?L-1 in a dose-dependent manner and significantly increased the cell survival rate following anoxia (P

AIM To investigate the protective effects and mechanism of propofol on cultured rat hippocampal neurons subjected to anoxia injury METHODS Hippocampal neurons of neonatal rats, which had been cultured in vitro for 10 days, were allocated to control groups and propofol treating groups In propofol treated groups,the culture medium were loaded with propofol at the concentrations of 3, 6, 12, 24, 48 mg?L -1 respectively, and then the neurons were exposed to oxygen glucose deprivation for 24 h, to 40 ?mol?L -1 H 2O 2 for 24 h or to 100 ?mol?L -1 glutamate for 50 min The cell survival rate in each group was evaluated by MTT colorimetry. Using a laser scanning confocal microscope (LSCM), the effects of propofol on neuronal calcium overload and on the reduction of mitochondrial membrane potential (△?m) evoked by anoxia were observed with fluo 3 and rhodamine 123 for real time changes of [Ca 2+ ] i and △?m. The electron spin resonance (ESR) was used to measure the scavenging effects of propofol on hydroxyl radical and superoxide anion RESULTS Propofol at the concentrations of 6～48 mg?L -1 attenuated the anoxic injury ( P

AIM: To explore the mechanism of nicotine against the apoptosis induced by colchicines in rat cortical neurons.METHODS: Cortical neurons were cultured from newborn Sprague-Dawley(SD) rats(less than 12 h).The rate of apoptosis was measured by Hoechst33258 fluorescence staining in the neurons,and the activity of Akt473 was analyzed by assay kit Akt473.RESULTS: The apoptosis of cortical neurons can be induced by 0.1 ?mol/L colchicine.The phosphorlation of Akt 473 decreased significantly(1/3 times of the control group,P

Aim To investigate the effect of the extract of Averrhoacarambola L.root (EACR)on renal func-tion in diabetic mice and its anti-oxidative action. Methods Diabetic mice were established by tail vein injection with 120 mg·kg-1 streptozotocin (STZ)and were divided into 5 groups:model control group,val-sartan control group,and low-,middle-,high-dose of EACR groups (300,600,1 200 mg·kg-1 ).And 10 normal mice consisted of normal control group.The fasting blood glucose (FBG)of mice was detected be-fore and after administration of drugs.After last admin-istration,the blood and urine samples were collected for creatinine (Cr),urea nitrogen (BUN),urine and 24 h urinary protein determination.The activities of superoxide dismutase (SOD ),glutathione peroxidase (GSH-Px)and malonaldehyde (MDA)content were determined using kits.HE staining was conducted to observe the pathological changes of kidney tissues. ELISA method was utilized to detect the contents of catalase (CAT)and reactive oxygen species (ROS ). The expressions of Cyto-C,AIF and caspase-3 proteins in kidney tissues were analyzed by Western blot.Re-sults Compared with model group,the serum bio-chemical indexes and 24 h urinary protein of valsartan and moderate-,high-dose of EACR groups were de-creased with statistical significance (P<0.05 ).After the treatment, the MDA content was decreased by EACR treatment,and SOD,GSH-Px and CAT activities were enhanced.Meanwhile the expressions of ROS, Cyto-C,AIF and caspase-3 were down-regulated.The pathological changes of kidney tissues were ameliorated by EACR through HE results.Conclusions The ex-tract of Averrhoacarambola L.root can decrease the se-rum levels of Cr and BUN,reduce the MDA and ROS contents in kidney tissue and enhance the activities of SOD,GSH-Px and CAT,down-regulate the expres-sions of Cyto-C,AIF and caspase-3 proteins in kidney tissues,elevate the anti-oxidative effect of kidney. Therefore,the renal function of diabetic mice is melio-rated.